prostate cancer is a leading cause of cancer deaths in men and still eludes medical treatment and prevention. It has been speculated that this is due to the lack of comprehensive understanding about the processes of normal development and growth of the prostate. Aberrations in growth and development are thought to be critical processes which lead to cancerous growths. Vitamin A is a key regulator of normal organ development and the major active form of vitamin A in this process is a derivative called retinoic acid. We propose that a reduction in retinoic acid efficacy may lead to abnormal development of the prostate. To test this theory, we will use the neonatally estrogenized rat prostate , a model which exhibits stromal hyperplasia, reduced ductal morphogenesis, and retarded epithelial differentiation during neonatal development. These developmental aberrations imprint upon subsequent prostate growth such that the adult estrogenized prostate forms preneoplastic lesions (dysplasisas and adenomas). We will evaluate whether the function of retinoic acid in this animal model is deficient by evaluating the levels of retinoic acid and its receptor in the prostate. To validate our theory, we will supplement retinoic acid to the neonatally estrogenized rats to demonstrate whether retinoic acid can prevent developmental aberrations associated with estrogen treatment. If retinoic acid prevents the development of preneoplastic lesions, then it may warrant future human studies to evaluate its role in the prevention of prostate cancer.